Journal
HAUTARZT
Volume 67, Issue 6, Pages 422-+Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00105-016-3800-8
Keywords
Th17; IL-23; Autoimmune diseases; Skin; Inflammation
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Psoriasis is an inflammatory T cell-mediated autoimmune disease of skin and joints that affects 2-4 % of the adult population and 0.1-1 % of children. Genetic susceptibility, environmental triggering factors, and innate immune processes initiate psoriasis pathogenesis that results in an adaptive autoreactive response. The T cell response is orchestrated by CD 8(+) T cells in the epidermis and by CD 4(+) T cells in the dermis that predominantly produce interleukin-17 (ILaEuro17). Research of the past 15 years unraveled cellular and molecular mechanisms as well as cytokines like TNF-alpha or ILaEuro23 that contribute to psoriatic inflammation. This knowledge has been translated into clinical practice and a number of antipsoriatic small molecules and immunobiologics are now available. Here, we discuss the current principles of psoriasis pathogenesis in the context of modern therapies.
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